Neural correlates of eating behaviour in obesity and after obesity surgery

Abstract

Background: Obesity is a serious, worldwide health concern. The urgent need to find an effective, safe and long-term treatment for this multifaceted chronic disease, requires a full and comprehensive understanding of its pathology. Indeed, eating behaviour is essential in understanding obesity development and consequently; is a key in optimising treatment. Functional magnetic resonance imaging (fMRI) has been recently utilized to understand the neural correlates of eating behaviour in obesity, specifically the reward system within the brain. Objectives: This thesis aimed to investigate the neural correlates of eating behaviour in obesity by examining the effect of: (i) obesity surgery, (ii) body mass index (BMI), and (iii) insulin resistance on food cue reactivity and other eating behaviour measures. Methods: Neural correlates of eating behaviour were examined by performing: (i) a comprehensive systemic review of functional magnetic resonance imaging (fMRI) studies after Roux-en Y gastric bypass (RYGB), vertical sleeve gastrectomy (VSG) and adjusted gastric band (AGB) surgeries; (ii) secondary analysis of three datasets to examine BMI and insulin resistance value as markers of food cue reactivity in three cohorts predominately consisting patients with obesity. Results: Findings from fMRI studies systematic review suggested the following: (i) after obesity surgery, specifically RYGB surgery, high-energy food cue reactivity sometimes decreased or else did not change in striatal, limbic and insula, regions implicated in reward processing. (ii) Although little evidence is available from VSG and AGB surgeries suggesting changes in food cue reactivity in brain regions involved in reward processing, a potential effect of VSG surgery on food cue reactivity in the dorsolateral prefrontal cortex. (iii) Some consistent evidence for a potential role for satiety gut hormones glucagon-like-peptide 1 (GLP-1) and peptide tyrosine tyrosine (PYY) in reduced food cue reactivity after RYGB surgery. Findings from secondary analysis of three datasets examining the effect of BMI on food cue reactivity revealed that contrary to expectations, no difference between groups in food cue 8 reactivity to high-energy food pictures in all cohorts. However, in participants with severe obesity compared to participant with non-severe obesity, lower food cue reactivity to low- energy food pictures in one cohort. Findings from secondary analysis of three datasets examining the effect of insulin resistance on food cue reactivity revealed that in participants with higher insulin resistance compared to participants with lower insulin resistance, higher food cue reactivity to high-energy vs. low- energy food pictures. However, these findings were only seen in one cohort and were not reproducible in the other two cohorts. Conclusion: In fMRI studies after obesity surgery, large methodological variation across studies, often with small numbers, with variable results of changes in food cue reactivity after obesity surgery, limits conclusions. Obesity surgeries, specifically RYGB and VSG, alter food cue reactivity in regions involved in reward processing and cognitive control. Heterogeneity in participants across the three cohorts limited findings replicability; however, findings suggest BMI as a potential marker for altered brain responses in regions implicated in reward processing in obesity. Moreover, altered food cue reactivity in obesity is not consistently seen as heightened reactivity for high energy food, it might be manifested as lower reactivity to low energy food. Finally, limited evidence for insulin resistance as a marker for food cue reactivity and other eating behaviour measures in obesity.